Biochemical And Clinical Indications For Liver Transplantation In Chronic Liver Disease

Indikasi Transplantasi Hati pada Penyakit Hati Kronik

Cholestatic Liver Disease

Bilirubin >10 mg/dL Intractable pruritus Progressive cholestatic bone disease Recurrent bacterial cholangitis

Hepatocellular Liver Disease

Serum albumin <3 g/dL Prothrombin time > 3 sec above control

Both Cholestatic And Hepatocellular Liver Diseases

Recurrent or severe hepatic encephalopathy Refractory ascites Spontaneous bacterial peritonitis Recurrent portal hypertensive bleeding Severe chronic fatigue and weakness Progressive malnutrition Development of hepatorenal syndrome Detection of small hepatocellular carcinoma

Referensi:
Cecil Medicine 23rd Edition (Saunders) 2008

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Liver Diseases Unique To Pregnancy

Penyakit Hati yang Berhubungan dengan Kehamilan

	Trimester of Onset	Symptoms	Laboratory Abnormalities	Recurrence with Future Pregnancies
Hyperemesis gravidarum	1	Nausea, vomiting	Mild to moderate elevation in AST/ALT, occasionally hyperbilirubinemia
Cholestasis	2, 3	Pruritus, jaundice	Bile acids >8 μM, elevated AST/ALT and bilirubin in more severe cases	Common
Acute fatty liver	3	Nausea, vomiting, abdominal pain	Elevated AST/ALT (100–1000 U/L), bilirubin >5 mg/dL, prolonged prothrombin time[*]	Rare
HELLP syndrome	2, 3, or postpartum	Abdominal pain, nausea, vomiting	Elevated AST/ALT (60–1500 U/L), platelets <100,000/mm3, LDH >600 U/L, hemolytic anemia	3–25%

Notes:

• ALT = alanine aminotransferase 
• AST = aspartate aminotransferase 
• HELLP = hemolysis, elevated liver enzymes, and low platelet count 
• LDH = lactate dehydrogenase  

Referensi:
Cecil Medicine 23rd Edition (Saunders) 2008

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Obstructive Jaundice Versus Cholestatic Liver Disease

Perbedaan antara Ikterik Obstruktif dengan Penyakit Hati Kolestatik

Feature	Suggests Obstructive Jaundice	Suggests Parenchymal Liver Disease
History	Abdominal pain	Anorexia, malaise, myalgias, suggestive of a viral prodrome
	Fever, rigors	Known infectious exposure
	Previous biliary surgery	Receipt of blood products, use of intravenous drugs
	Older age	Exposure to a known hepatotoxin
	Acholic stools	Family history of jaundice
Physical examination	High fever	Ascites
	Abdominal tenderness	Other stigmata of liver disease (e.g., prominent abdominal veins, gynecomastia, spider angiomas, asterixis, encephalopathy, Kayser-Fleischer rings)
	Palpable abdominal mass
	Abdominal scar
Laboratory studies	Predominant elevation of serum bilirubin and alkaline phosphatase	Predominant elevation of serum aminotransferases
	Prothrombin time that is normal or normalizes with vitamin K administration	Prolonged prothrombin time that does not correct with vitamin K administration
	Elevated serum amylase	Blood tests indicative of specific liver disease

Referensi:
Cecil Medicine 23rd Edition (Saunders) 2008

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Drug Treatment Of Asthma During Pregnancy

Penatalaksanaan Asma Selama Kehamilan

Therapy	Comments
Desensitization or immunotherapy (“allergy shots”)	Ongoing therapy can be continued. However, skin testing, initiating treatment, and increasing therapy should be avoided. Reducing exposure to environmental irritants and allergens remains important.
Antihistamines (chlorpheniramine and tripelennamine preferred and nonsedating agents used when sedation must be minimized)	More information is available for older antihistamines. Recommendations for newer agents, with less sedation, are based on limited animal and human data.
Disodium cromoglycate and nedocromil	Less than 10% of the drug is absorbed. No reported adverse effects from use during pregnancy.
Theophylline	Distribution and clearance are altered during pregnancy, and levels should be checked monthly. It crosses the placenta; rarely, neonatal toxicity has been reported despite therapeutic maternal levels.
β -Agonists (albuterol, metaproterenol, terbutaline; no data on salmeterol)	Use is safe during pregnancy. Rare reports of tocolytic effects.
Inhaled ipratropium	Little data on use during pregnancy, although it is probably safe.
Antileukotriene (zafirlukast, montelukast, zileuton)	No human information; zileuton had adverse effects in animal studies and is not recommended for use during pregnancy.
Inhaled corticosteroids (beclomethasone and budesonide best studied)	Regular use reduces asthma exacerbations during pregnancy.
Oral corticosteroids	May be used safely when indicated. Ninety percent of prednisone is inactivated by the placenta, thus reducing fetal exposure. Betamethasone does not undergo placental 11-oxidation and is the preferred corticosteroid when promoting fetal lung maturation.

Referensi:
Cecil Medicine 23rd Edition (Saunders) 2008

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Antihypertensive Drug Use During Pregnancy

Obat-Obat Antihipertensi Selama Kehamilan

Medication	Safety of Use during Pregnancy	Comments
CENTRAL SYMPATHOLYTIC
Methyldopa	++++	Extensive use, most studied, and best safety record of any antihypertensive used during pregnancy. It reduces vascular resistance while preserving maternal cardiac output and uteroplacental perfusion. Considered safe to use when breast-feeding
Clonidine	+++	Not assessed for chronic hypertension during pregnancy. No adverse effects when used for hypertension during the third trimester. Potential for rebound when discontinued abruptly
α- AND β-BLOCKERS
Labetalol	++++	Used in several trials without adverse effects. α-Blocking results in vasodilation (including uteroplacental blood vessels), and β -blockade prevents reflex tachycardia. Cardiac output is unchanged. Low concentration in breast milk
β-BLOCKERS
Atenolol, metoprolol, pindolol, propranolol	+++	Probably safe for third-trimester use, but neonatal bradycardia, respiratory distress, and hypoglycemia have been reported. Use earlier in gestation may result in intrauterine growth retardation. Atenolol and metoprolol are concentrated in breast milk; propranolol has low concentrations in breast milk
DIRECT ARTERIAL VASODILATOR
Hydralazine	++++	Extensively used during pregnancy. It causes vascular dilation and reflex tachycardia. Primarily used parenterally for acute management of hypertension or with methyldopa or a β-blocking agent
CALCIUM-CHANNEL BLOCKERS
Nifedipine (most commonly used because of its primarily peripheral effects), diltiazem, verapamil	+++	Probably safely used in the third trimester. Their use maintains uteroplacental perfusion; may also have tocolytic effects. Sublingual nifedipine has been associated with hypotension and fetal distress. Avoid use with magnesium sulfate because combination risks profound hypotension
DIURETICS
Hydrochlorothiazide, chlorthalidone, furosemide	++	Use during pregnancy is controversial and often discontinued as blood pressure decreases early in pregnancy. If used before pregnancy, it can be continued, but its use should not be initiated during pregnancy. Concentrations in breast milk are low. May reduce milk production
ANGIOTENSIN-CONVERTING ENZYME INHIBITORS AND ANGIOTENSIN II RECEPTOR BLOCKERS
Captopril, lisinopril, benazepril, enalapril, losartan, valsartan, candesartan	0	Use is contraindicated during pregnancy because it affects renal development in the second and third trimesters. Miscarriage, fetal death, malformations, and neonatal renal failure can result. No reports of adverse effects from brief use, limited to the first trimester. Few data on the effects of angiotensin II receptor antagonists, but presumed similar and also contraindicated

Drugs listed have established effects during pregnancy. Antihypertensive agents not listed may be safe during pregnancy; however, until safety is known, those drugs should be switched to one of the safely used listed agents. 

Referensi:
Cecil Medicine 23rd Edition (Saunders) 2008

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Differential Diagnosis Of Chronic Hepatitis

Diagnosis Banding Hepatitis Kronik

Diagnosis	Screening Tests	Confirmatory Tests (Serum or Liver)	Comments
Chronic hepatitis B	HBsAg	HBV DNA, HBeAg, or HBcAg in liver
Chronic hepatitis C	Anti-HCV	HCV RNA (using PCR)	Immunoblot for anti-HCV can be used to confirm antibody reactivity
Chronic hepatitis D	Anti-HDV	HDV RNA or HDV antigen in the liver
Autoimmune hepatitis	ANA (anti-LKM1)	Exclusion of other causes and patterns of clinical disease	Suggested by raised IgG levels and by response to corticosteroid therapy
Drug-induced liver disease	History	Rechallenge, if necessary, is considered safe	Medications most suspected include isoniazid, NSAIDs, methyldopa, nitrofurantoin
Wilson's disease	Ceruloplasmin	Urine and hepatic copper concentration	Suggested by hemolysis or severe chronic hepatitis in a child or adolescent
Cryptogenic	Exclusion of other causes		Major differential is with autoimmune hepatitis and drug-induced liver disease

Notes: ANA = antinuclear antibody anti-LKM1 = liver-kidney microsomal 1 antibody HBcAg = hepatitis B core antigen HBeAg = hepatitis B e antigen HBsAg = hepatitis B surface antigen HBV = hepatitis B virus  HCV = hepatitis C virus HDV = hepatitis D virus IgG = immunoglobulin G  NSAIDs = nonsteroidal anti-inflammatory drugs  Referensi: Cecil Medicine 23rd Edition (Saunders) 2008 Download table

Differential White Cell Counts (WCC): Acute Fever In The Absence Of Localising Signs

Perbedaan Hitung Jenis Lekosit Pada Demam Akut

WCC differential	Potential diagnoses	Futher investigations
Neutrophil leucocytosis	Bacterial sepsis Leptospira and Borrelia infections   Leptospirosis   Tick-borne   relapsing feve   Louse-borne   relapsing feverr Amoebic liver abscess	Blood culture Culture of blood and urine, serology Blood film Blood film Ultrasound
Normal WCC and differential	Typhoid fever Typhus Arboviral infection	Blood, stool and urine culture Serology Serology (PCR and viralculture)
Lymphocytosis	Viral fevers Infectious mononucleosis Rickettsial fevers	Serology Monospot test Serology

Referensi:
Davidson's Principles and Practice of Medicine 20th Edition (Churchill Livingstone) 2007

Glycogen Storage Diseases (GSD): Clinical features and Complications

GSD	Eponym	Enzyme defect	Clinical features and complications
I	Von Gierke	Glucose-6-phosphatase deficiency	Childhood presentation, hypoglycaemia, hepatomegaly
II	Pompe	α-glucosidase (acid maltase) deficiency	Classical presentation in infancy, muscle weakness (may be severe)
III	Cori	Debrancher enzyme deficiency	Childhood presentation, hepatomegaly, mild hypoglycaemia
IV	Andersen	Brancher enzyme deficiency	Presentation in infancy, severe muscle weakness (may affect heart), cirrhosis
V	McArdle	Muscle glycogen phosphorylase deficiency	Exercise-induced fatigue and myalgia
VI	Hers	Liver phosphorylase deficiency	Mild hepatomegaly
VII	Tarui	Muscle phosphofructokinase deficiency	Exercise-induced fatigue and myalgia
VIII		Liver phosphorylase kinase deficiency	Very mild disease; hepatomegaly, growth retardation, elevated hepatic enzymes, hyperlipidaemia, fasting hyperketosis
IX		Liver glycogen phosphorylase kinase deficiency	Mild hepatomegaly. Inheritance can be autosomal or X-linked recessive
0		Hepatic glycogen synthase deficiency	Fasting hypoglycaemia, post-prandial hyperglycaemia

Referensi:
Davidson's Principles & Practice of Medicine 20th Edition (Churchill Livingstone) 2007

Common Oral Antianginal Drugs

Obat-Obat Anti Angina 

Drug Usual Dose Comments; Adverse Effects Nitrates   Nitroglycerin 0.4–0.6 mg SL Aborts acute attacks; headaches, hypotension Nitroglycerin 1–3 mg buccal Larger tablet for handicapped patients Nitroglycerin 0.4 mg spray More convenient than pills Nitroglycerin 0.5–2 in of 2% ointment Prophylactic therapy; tolerance a problem Nitroglycerin 0.1–0.6 mg/h patches Prophylactic therapy; tolerance a problem Isosorbide dinitrate 10–60 mg three times daily Need 8 h off q24h to avoid tolerance Isosorbide mononitrate 20 mg twice daily Take 7 h apart Drug   Daily Dosage (mg)   Comments; Adverse Effects   –Blockers   Propranolol 160–320 CNS side effects—fatigue, impotence—common Nadolol 80–240 Long half-life, noncardioselective Timolol 10–45 Noncardioselective Metaprolol 100–400 Cardioselective Atenolol 50–200 Cardioselective Acebutolol 400–1200 Cardioselective, some intrinsic sympathomimetic activity Betaxolol 5–40 Cardioselective, long half-life Bisoprolol 5–20 Cardioselective Pindolol 5–40 Marked intrinsic sympathomimetic activity Calcium Channel Blockers, Heart Rate Lowering   Diltiazem 120–360 Heart-rate lowering; AV block, heart failure, edema Verapamil 120–480 Heart-rate lowering; AV block, heart failure, constipation Dihydroperidine Calcium Channel Blockers   Amlodipine 5–10 Least myocardial depression Nifedipine 30–60 Hypotension, tachycardia Nicardipine 60–120 Potent coronary vasodilator Felodipine 5–20 High vascular selectivity Isradipine 2.5–10 Potent coronary vasodilator Nisoldipine 10–40 Similar to nifedipine Sodium Current Inhibitor   Ranolazine 1000–2000 mg May increase QT interval on ECG

Referensi:
Current Diagnosis & Treatment Cardiology 3rd Edition (McGraw-Hill) 2009

Comparison Of Haemodialysis And Peritoneal Dialysis

Perbandingan (Perbedaan) antara Hemodialisis dengan Dialisis Peritoneal

Haemodialysis	Peritoneal dialysis
Efficient	Less efficient
4 hours three times per week usually adequate	Four exchanges per day usually required, each taking 30-60 minutes (continuous ambulatory peritoneal dialysis) or 8-10 hours each night (automated peritoneal dialysis)
2-3 days between treatments	A few hours between treatments
Requires visits to hospital (although home treatment possible for some patients)	Performed at home
Requires adequate venous circulation for vascular access	Requires an intact peritoneal cavity without major scarring from previous surgery
Careful compliance with diet and fluid restrictions required between treatments	Diet and fluid less restricted
Fluid removal compressed into treatment periods; may cause symptoms and haemodynamic instability	Slow continuous fluid removal, usually asymptomatic
Infections related to vascular access may occur	Peritonitis and catheter-related infections may occur
Patients are to some extent dependent on others	Patients can take full responsibility for their treatment

Referensi:
Davidson's Principles & Practice of Medicine 20th Edition (Churchill Livingstone) 2007

Eruption Pattern of Teeth

Pola Erupsi Gigi

Teeth Eruption Date Primary dentition    Mandibular central incisor 6 mo   Maxillary central incisor 7 mo   Mandibular lateral incisor 7 mo   Maxillary lateral incisor 9 mo   Mandibular first molar 12 mo   Maxillary first molar 14 mo   Mandibular canine 16 mo   Maxillary canine 18 mo   Mandibular second molar 20 mo   Maxillary second molar 24 mo Permanent dentition    Mandibular central incisors 6 y   Maxillary first molars 6 y   Mandibular first molars 6 y   Maxillary central incisors 7 y   Mandibular lateral incisors 7 y   Maxillary lateral incisors 8 y   Mandibular canines 9 y   Maxillary first premolars 10 y   Mandibular first premolars 11 y   Maxillary second premolars 11 y   Mandibular second premolars 11 y   Maxillary canines 11 y   Mandibular second molars 12 y   Maxillary second molars 12 y   Mandibular third molars 17–21 y   Maxillary third molars 17–21 y

Referensi:
Current Diagnosis & Treatment Family Medicine 2nd Edition (McGraw-Hill) 2007

Correlations Between CD4 Count and HIV-Associated Diseases

CD4 Count > 500 cells/mm3

• Acute primary infection
• Recurrent vaginal candidiasis
• Persistent generalised lymphadenopathy

CD4 Count < 500 cells/mm3

• Pulmonary tuberculosis
• Pneumococcal pneumonia
• Herpes zoster
• Oropharyngeal candidiasis
• Oral hairy leucoplakia
• Extra-intestinal salmonellosis
• Kaposi's sarcoma
• HIV-associated idiopathic thrombocytopenic purpura
• Cervical intra-epithelial neoplasia II-III
• Lymphoid interstitial pneumonitis

CD4 Count < 200 cells/mm3

• Pneumocystis carinii (jirovecii) pneumonia
• Mucocutaneous herpes simplex
• Cryptosporidium
• Microsporidium
• Oesophageal candidiasis
• Miliary/extrapulmonary tuberculosis
• HIV-associated wasting
• Peripheral neuropathy

CD4 Count < 100 cells/mm3

• Cerebral toxoplasmosis
• Cryptococcal meningitis
• Primary CNS lymphoma
• Non-Hodgkin lymphoma
• HIV-associated dementia
• Progressive multifocal leucoencephalopathy

CD4 Count < 50 cells/mm3

• CMV retinitis/gastrointestinal disease
• Disseminated Mycobacterium avium intracellulare

Referensi:
Davidson's Principles & Practice of Medicine 20th Edition (Churchill Livingstone) 2007

Indications and Contraindications for Implantable Cardioverter Defibrillator Therapy

Randomized trials have indicated that ICD therapy for primary prevention of sudden death is effective in many populations. The current indications for ICD insertion accepted by the Center for Medicare Services are shown in Table below. The most recent trials have used entry criteria based primarily on left ventricular ejection fraction (below 30% or 35%) and NYHA functional class. Most primary prevention trials have reported relative risk reductions in a range similar to those seen in the secondary prevention trials (20–30%). The CABG-Patch Trial and the Defibrillators in Acute Myocardial Infarction Trial (DINAMIT) failed to show benefit in patients who received their ICD either at the time of coronary revascularization or within 40 days of an acute myocardial infarction, respectively. These trials resulted in the specific exclusion of these conditions in the current guidelines. 

Indications and Contraindications for Implantable Cardioverter Defibrillator Therapy

I. Indications for Secondary Prevention   A. Documented episode of cardiac arrest due to ventricular fibrillation (VF), not due to a transient or reversible cause   B. Documented sustained ventricular tachyarrhythmia (VT), either spontaneous or induced by an electrophysiology (EP) study, not associated with an acute myocardial infarction (MI) and not due to a transient or reversible cause II. Indications for Primary Prevention   A. Documented familial or inherited conditions with a high risk of life-threatening VT, such as long QT syndrome or hypertrophic cardiomyopathy   B. Coronary artery disease with a documented prior MI, a measured left ventricular ejection fraction (LVEF) < 35%, and inducible, sustained VT or VF at EP study. (The EP test must be performed more than 4 weeks after the qualifying MI.)   C. Documented prior MI and a measured LVEF < 30%   D. Patients with ischemic dilated cardiomyopathy, documented prior MI, New York Heart Association (NYHA) class II and III heart failure, and measured LVEF < 35%   E. Patients with nonischemic dilated cardiomyopathy > 9 months, NYHA class II and III heart failure, and measured LVEF < 35%   F. Patients who meet all current Centers for Medicare & Medicaid Services coverage requirements for a cardiac resynchronization therapy (CRT) device and have NYHA class IV heart failure   G. Patients with nonischemic dilated cardiomyopathy > 3 months, NYHA class II and III heart failure, and measured LVEF < 35% III. Exclusions   A. NYHA classification IV without CRT   B. Cardiogenic shock or symptomatic hypotension while in a stable baseline rhythm   C. Had a coronary artery bypass graft or percutaneous transluminal coronary angioplasty within past 3 months   D. Had an enzyme positive MI within past 40 days   E. Clinical symptoms or findings that would make them a candidate for coronary revascularization   F. Any disease, other than cardiac disease (eg, cancer, uremia, liver failure), associated with a likelihood of survival less than 1 year   G. Patients must not have irreversible brain damage from preexisting cerebral disease

Referensi:
Current Diagnosis & Treatment Cardiology 3rd Edition (McGraw-Hill) 2009

Clinical Overview of Current Inhaled Anesthetics: Isoflurane, Desflurane, Sevoflurane, Xenon, Nitrous Oxide

Isoflurane
Isoflurane is a halogenated methyl ethyl ether that is a clear, nonflammable liquid at room temperature and has a high degree of pungency. It is the most potent of the volatile anesthetics in clinical use, has great physical stability, and undergoes essentially no deterioration during storage for up to 5 years or on exposure to sunlight. It has become the “gold standard” anesthetic since its introduction in the 1970s. There was a brief period of controversy concerning the use of isoflurane in patients with coronary disease because of the possibility for coronary “steal” arising from the potent effects of isoflurane on coronary vasodilation. In clinical use, however, this has been, at most, a rare occurrence.

Desflurane
Desflurane is a fluorinated methyl ethyl ether that differs from isoflurane by just one atom: a fluorine atom is substituted for a chlorine atom on the α-ethyl component of isoflurane. The process of complete fluorination of the ether molecule has several effects. It decreases blood and tissue solubility (the blood:gas solubility of desflurane equals that of nitrous oxide), and it results in a loss of potency (the MAC of desflurane is 5 times higher than isoflurane). Moreover, fluorination of the methyl ether molecule results in a high vapor pressure owing to decreased intermolecular attraction. Thus, a new vaporizer technology was developed to deliver a regulated concentration of desflurane as a gas. It is a heated, pressurized vaporizer requiring electrical power and more frequent servicing. One of the advantages of desflurane is the near-absent metabolism to serum trifluoroacetate. This makes immune-mediated hepatitis a rare occurrence. Desflurane is the most pungent of the volatile anesthetics, and if administered via the face mask results in coughing, salivation, breath holding, and laryngospasm. In extremely dry CO2 absorbers, desflurane (and to a lesser extent isoflurane, enflurane, and sevoflurane) degrades to form carbon monoxide. Desflurane has the lowest blood:gas solubility of the potent volatile anesthetics; moreover, its fat solubility is roughly half of that of the other volatile anesthetics. Thus, desflurane requires less downward titration in long surgical procedures to achieve a rapid emergence by virtue of decreased tissue saturation. Desflurane has been associated with tachycardia, hypertension, and, in select cases, myocardial ischemia when used in high concentrations or rapidly increasing the inspired concentration (without using opioid adjuvants to prevent such a response).


Sevoflurane
Sevoflurane is a sweet-smelling, completely fluorinated methyl isopropyl ether. Its vapor pressure is roughly one-fourth that of desflurane and it can be used in a conventional vaporizer. The blood:gas solubility of sevoflurane is second only to desflurane in terms of potent volatile anesthetics. Sevoflurane is approximately half as potent as isoflurane, and some of the preservation of potency, despite fluorination, is because of the bulky propyl side chain on the ether molecule. Sevoflurane has minimal odor, no pungency, and is a potent bronchodilator. These attributes make sevoflurane an excellent candidate for administration via the face mask on induction of anesthesia in both children and adults. Sevoflurane is half as potent a coronary vasodilator as isoflurane, but is 10 to 20 times more vulnerable to metabolism than isoflurane. The metabolism of sevoflurane results in inorganic fluoride; the increase in plasma fluoride after sevoflurane administration has not been associated with renal-concentrating defects. Unlike other potent volatile anesthetics, sevoflurane is not metabolized to trifluoroacetate; rather, it is metabolized to an acyl halide (hexafluoroisopropanol). This does not stimulate formation of antibodies.
Sevoflurane can form carbon monoxide during exposure to dry CO2 absorbents, and an exothermic reaction in dry absorbent has resulted in canister fires. New generic versions of sevoflurane have the potential to break down to hydrogen fluoride when exposed to metal compounds because of their lack of adequate water in the formulation. Sevoflurane also breaks down in the presence of the carbon dioxide absorber to form a vinyl halide called compound A. Compound A has been shown to be a dose-dependent nephrotoxin in rats, but has not been associated with renal injury in human volunteers or patients, with or without renal impairment, even when fresh gas flows are 1 L/min or less.


Xenon 
Xenon is an inert gas. Difficult to obtain, and hence extremely expensive, it has received considerable interest in the last few years because it has many characteristics approaching those of an “ideal” inhaled anesthetic, although it can trigger malignant hyperthermia. Its blood:gas partition coefficient is 0.14, and unlike the other potent volatile anesthetics (except methoxyflurane), xenon provides some degree of analgesia. The MAC of xenon in humans is 71%, which might prove to be a limitation. It is nonexplosive, nonpungent, and odorless, and thus can be inhaled with ease. In addition, it does not produce significant myocardial depression. Because of its scarcity and high cost, new anesthetic systems need to be developed to provide for recycling of xenon. If this proves to be too difficult from either a technical or patient safety standpoint, it may be necessary to use it in a very low, or closed, fresh gas flow system to reduce wastage.

Nitrous Oxide
Nitrous oxide is a sweet-smelling, nonflammable gas of low potency (MAC = 104%) and is relatively insoluble in blood. It is most commonly administered as an anesthetic adjuvant in combination with opioids or volatile anesthetics during the conduct of general anesthesia. Although not flammable, nitrous oxide will support combustion. Unlike the potent volatile anesthetics in clinical use, nitrous oxide does not produce significant skeletal muscle relaxation, but it does have documented analgesic effects. Despite a long track record of use, controversy has surrounded nitrous oxide in four areas: its role in postoperative nausea and vomiting, its potential toxic effects on cell function via inactivation of vitamin B12, its adverse effects related to absorption and expansion into air-filled structures and bubbles, and lastly, its effect on embryonic development. The one concern that seems most valid and most clinically relevant is the ability of nitrous oxide to expand air-filled spaces because of its greater solubility in blood compared to nitrogen. Several closed gas spaces, such as the bowel and middle ear, exist in the body and other spaces may occur as a result of disease or surgery, such as a pneumothorax. Because nitrogen in air-filled spaces cannot be removed readily via the bloodstream, nitrous oxide delivered to a patient diffuses from the blood into these closed gas spaces quite easily. Movement of nitrous oxide into these spaces continues until the partial pressure equals that of the blood and alveoli. Compliant spaces will continue to expand until sufficient pressure is generated to oppose further nitrous oxide flow into the space. The higher the inspired concentration of nitrous oxide, the higher the partial pressure required for equilibration.
Seventy-five percent nitrous oxide can expand a pneumo-thorax to double or triple its size in 10 and 30 minutes, respectively. Air-filled cuffs of pulmonary artery catheters and endotracheal tubes also expand with the use of nitrous oxide, possibly causing tissue damage via increased pressure in the pulmonary artery or trachea, respectively. In a rabbit model, the volume of an air embolus resulting in cardiovascular compromise is less during coadministration of nitrous oxide. Accumulation of nitrous oxide in the middle ear can diminish hearing postoperatively and is relatively contraindicated for tympanoplasty because the increased pressure can dislodge a tympanic graft.

Referensi: 

Barash's Clinical Anesthesia 6th Edition (Lippincott Williams & Wilkins) 2009

Drugs That Have Been Associated with Significant Effects on Some Nursing Infants

Obat-Obatan yang Sebaiknya Dihindari oleh Ibu Menyusui

Drug Reported Effecta Acebutolol Hypotension, bradycardia, tachypnea 5-Aminosalicylic acid Diarrhea (one case) Atenolol Cyanosis, bradycardia Bromocriptine Suppresses lactation, may be hazardous to the mother Aspirin (salicylates) Metabolic acidosis (one case) Clemastine Drowsiness, irritability, refusal to feed, high-pitched cry, neck stiffness (one case) Ergotamine Vomiting, diarrhea, convulsions—doses used in migraine medications Lithium A third to half therapeutic blood concentration in infants Phenindione Anticoagulant—increased prothrombin and partial thromboplastin time in one infant—not used in United States Phenobarbital Sedation; infantile spasms after weaning from milk containing phenobarbital; methemoglobinemia (one case) Primidone Sedation, feeding problems Sulfasalazine Bloody diarrhea (one case)

aBlood concentration in the infant may be of clinical importance.

Referensi:
Williams Obstetrics 23rd Edition (McGraw-Hill) 2009

Criteria for the diagnosis of rheumatoid arthritis

Kriteria Diagnosis Artritis Reumatoid (AR)

American Rheumatism Association 1958 criteria American College of Rheumatology 1987 criteria 1. Morning stiffness 1. Morning stiffness of at least 1 h in three or more joints 2. Pain on motion or tenderness in at least one joint 2. Arthritis of three or more joint areas 3. Swelling of one joint representing soft tissue or fluid 3. Arthritis of hand joints 4. Swelling of at least one other joint 4. Symmetric arthritis 5. Symmetric joint swelling 5. Rheumatoid nodules 6. Subcutaneous nodules 6. Serum rheumatoid factor positive 7. Typical radiologic arthritic changes 7. Typical radiographic changes in the hand and wrist 8. Positive test for rheumatoid factor in serum 9. Poor mucin precipitate from synovial fluid 10. Characteristic histologic changes in synovial membrane 11. Characteristic histopathology of rheumatoid nodules

Referensi:
Arthritis & Allied Conditions 15th Edition (Lippincott Williams & Wilkins) 2005

Summary of HIV-Associated Cardiovascular Diseases

Penyakit Jantung yang Berhubungan dengan HIV

Disease Type	Possible Causes	Incidence/Prevalence	Diagnosis	Treatment
Dilated cardiomyopathy	Drug-related: cocaine, AZT, IL-2, doxorubicin, interferon    Infectious: HIV, Toxoplasma, coxsackievirus group B, EBV, CMV, adenovirus    Metabolic or endocrine: selenium or carnitine deficiency, anemia, hypo-calcemia, hypophos-phatemia, hyponatremia, hypokalemia, hypo-albuminemia, hypo-thyroidism, growth hormone deficiency, adrenal insufficiency, hyper-insulinemia, hemochromatosis, pheochromocytoma, sarcoidosis, amyloidosis    Cytokines: TNF-α, nitric oxide, TGF-β, endothelin-I, interleukins    Immunodeficiency: CD4 < 100 cells/mm3    Autoimmune	Up to 8% of asymptomatic patients    Up to 25% of autopsy cases    Systolic > diastolic	Chest radiographic findings: non-specific conduction abnormalities, PVCs, PACs    Echocardiographic findings: low-normal LV wall thickness, increased LV mass, dilated LV, systolic LV dysfunction    Possible laboratory studies: troponin T, brain natriuretic peptide level, CD4 count, viral load, viral PCR, Toxoplasma serology, thyroid-stimulating hormone, cortisol, carnitine, selenium, serum ACE, vanillylmandelic acid, amyloid, urine analysis, stress testing, myocardial biopsy, cardiac catheterization	Diuretics, digoxin, ACE inhibitors, beta blockers    Adjunctive treatment in HIV patients: treatment of infection; nutritional replacement; IVIG; intensify antiretroviral therapy    Follow-up: serial echocardiography
Pericardial	Bacteria: Staphylococcus, Streptococcus, Proteus, Klebsiella, Enterococcus, Listeria, Nocardia, Mycobacterium    Viral pathogens: HIV, HSV, CMV, adenovirus, echovirus    Other pathogens: Cryptococcus, Toxoplasma, Histoplasma    Malignancy: Kaposi sarcoma, lymphoma, capillary leak, wasting, malnutrition    Hypothyroidism    Immunodeficiency    Uremia	11%/year, spontaneous resolution in 42% of affected patients; ∼ 30% increase in 6-month mortality	Pericardial rub on examination    Echocardiography    Fluid analysis for Gram stain and culture, cytology    ECG: low voltage, PR depression    Associated pleural and peritoneal fluid analysis    Pericardial biopsy	Treat the cause Follow-up: serial echocardiography; intensify antiretroviral therapy; pericardiocentesis or window
Infective endocarditis	Autoimmune    Bacteria: Staphylococcus aureus or S. epidermidis, Salmonella, Streptococcus, Haemophilus para-influenzae, Pseudallescheria boydii, HACEK    Fungal: Aspergillus fumigatus, Candida, Cryptococcus neoformans	6% increased incidence in IVDA, regardless of HIV status	Blood cultures; echocardiography	IV antibiotics, valve replacements
Nonbacterial thrombotic endocarditis	Valvular damage, vitamin C deficiency, malnutrition, wasting, DIC, hypercoagulable state, prolonged acquired immunodeficiency	Rare but clinically relevant emboli in 42% of cases	Echocardiography	Anticoagulation, treat vasculitis or underlying illness
Malignancy	Kaposi sarcoma, non–Hodgkin lymphoma, leiomyosarcoma, low CD4 count, prolonged immunodeficiency, HHV-8, EBV	Approximately 1% incidence, usually metastatic in HIV-positive patients	Echocardiography, biopsy	Chemotherapy possible
Right ventricular and pulmonary disease	Recurrent pulmonary infections, pulmonary arteritis, microvascular pulmonary emboli		ECG, echocardiog-raphy, right heart catheterization	Diuretics, treat underlying lung infection or disease, anticoagulation
Primary pulmonary hypertension	Plexogenic pulmonary arteriopathy	0.5%	ECG, echocardiog-raphy, right heart catheterization	Anticoagulation, vasodilators, prostacyclin analogues
Vasculitis	Drug therapy with antibiotics and antivirals	Increasing incidence	Clinical diagnosis	Systemic corticosteroids, withdrawal of drug
Accelerated atherosclerosis	Protease inhibitors, atherogenesis with virus-infected macrophages, chronic inflammation, glucose intolerance, dyslipidemia	Up to 8% prevalence	Stress testing, echocardiography, lipid profile, CT angiography, calcium scoring	Minimize risk factors
Autonomic dysfunction	CNS disease, drug therapy, prolonged immunodeficiency, malnutrition	Increased in patients with CNS disease	Tilt-table test, Holter monitoring	Procedural precautions
Arrhythmias	Drug therapy, pentamidine, autonomic dysfunction, acidosis, electrolyte abnormalities		ECG: long QT, Holter monitoring, exercise stress testing	Discontinue drug, procedural precautions
Lipodystrophy	Drug therapy: protease inhibitors		Echocardiography, lipid profile, cardiac catheterization, coronary calcium score	Lipid therapy (beware of drug interactions), aerobic exercise, altered antiretroviral therapy, cosmetic surgery, fat implantation

ACE = angiotensin-converting enzyme; AZT = azidothymidine; CMV = cytomegalovirus; CNS = central nervous system; DIC = disseminated intravascular coagulation; EBV = Epstein-Barr virus; ECG = electrocardiogram; HHV = human herpesvirus; HIV = human immunodeficiency virus; HSV = herpes simplex virus; HTN = hypertension; IL-2 = interleukin-2; IVDA = intravenous drug abuse; IVIG = intravenous immunoglobulin; LV = left ventricular; PAC = premature atrial complex; PCR = polymerase chain reaction; PVC = premature ventricular complex; TGF = transforming growth factor; TNF = tumor necrosis factor.

Referensi:
Braunwald's Heart Disease 8E (Saunders) 2007

Classification Criteria For Sjögren's Syndrome

		I. OCULAR SYMPTOMS
		A positive response to at least one of the three selected questions:    1.    Have you had daily, persistent, troublesome dry eyes for more than 3 months?    2.    Do you have a recurrent sensation of sand or gravel in the eyes?    3.    Do you use tear substitutes more than three times a day?
		II. ORAL SYMPTOMS
		A positive response to at least one of the three selected questions:    1.    Have you had a daily feeling of dry mouth for more than 3 months?    2.    Have you had recurrent or persistently swollen salivary glands as an adult?    3.    Do you frequently drink liquids to aid in swallowing dry food?
		III. OCULAR SIGNS
		Objective evidence of ocular involvement defined as a positive result in at least one of the following two tests:    1.    Schirmer's test (≤5 mm in 5 minutes)    2.    Rose bengal score (≥4 according to van Bijsterveld scoring system)
		IV. HISTOPATHOLOGY
		A focus score ≥1 in a minor salivary gland biopsy specimen. (A focus is defined as an agglomerate of at least 50 mononuclear cells; the
		focus score is defined by the number of foci in 4 mm2 of glandular tissue.)
		V. SALIVARY GLAND INVOLVEMENT
		Objective evidence of salivary gland involvement defined by a positive result in at least one of the following three diagnostic tests:    1.    Salivary scintigraphy    2.    Parotid sialography    3.    Unstimulated salivary flow (≤1.5 mL in 15 minutes)
		VI. AUTOANTIBODIES
		Presence in the serum of the following autoantibodies:    1.    Antibodies to Ro (SSA) or La (SSB) antigens, or both
		RULES FOR CLASSIFICATION
		In patients without any potentially associated disease, primary SS is diagnosed if    1.    4 of 6 criteria are met but including IV or VI    2.    3 of 4 of criteria III, IV, V, VI
		For secondary SS criteria, I or II plus any 2 of criteria III, IV, V should be met.
		EXCLUSION CRITERIA
		Preexisting lymphoma,  acquired immunodeficiency syndrome,  sarcoidosis,  graft-versus-host disease,  past head and neck radiation treatment,  use of anticholinergic drugs, and  hepatitis C

Referensi:
Cecil Medicine 23rd Edition (Saunders) 2008

Clinical Features and Clusters of 10 DSM-IV-TR Personality Disorders

Gambaran Klinik dan Jenis-Jenis Gangguan Kepribadian 

Personality disorders (PDs) are a heterogeneous group of deeply ingrained and enduring behavioral patterns characterized by inflexible and extreme responses to a broad range of situations, manifesting in cognition (ways of perceiving and interpreting self, others, and events), affectivity (range, intensity, lability, and appropriateness of response), interpersonal functioning, and impulse control. PDs impinge on medical practice in multiple ways, including self-destructive behaviors, interpersonal disturbances, and nonadherence. Appropriate physician responses and effective treatments exist for many PDs. Borderline personality disorder (BPD) is an extremely debilitating and notoriously difficult to treat disorder. BPD may be misattributed to other PDs, and behaviors of patients in crises may also misleadingly suggest BPD. Correct diagnosis of PDs and proper intervention will help to improve patient outcomes. 

Ten PDs are currently distinguished clinically. They are often grouped into three clusters: odd or eccentric (cluster A); dramatic, emotional, or erratic (cluster B); and anxious or fearful (cluster C). These groupings are helpful in broadly categorizing PD difficulties but are limited in their usefulness because they do not signify similarities in etiologies and treatment response.

Clinical Features and Clusters of 10 DSM-IV-TR Personality Disorders

Cluster Personality Disorder Clinical Features Cluster A: odd, eccentric Paranoid Suspicious; overly sensitive; misinterpretations Schizotypal Detached; perceptual and cognitive distortions; eccentric behavior Schizoid Detached; introverted, constricted affect Cluster B: dramatic, emotional, erratic Antisocial Manipulative; selfish, lacks empathy; explosive anger; legal problems since adolescence Borderline Dependent and demanding; unstable interpersonal relationships, self-image, and affects; impulsivity; micropsychotic symptoms Histrionic Dramatic; attention seeking and emotionality; superficial, ie, vague and focused on appearances Narcissistic Self-important; arrogance and grandiosity; need for admiration; lacks empathy; rages Cluster C: anxious, fearful Avoidant Anxiously detached; feels inadequate; hypersensitive to negative evaluation Dependent Clinging, submissive, and self-sacrificing; needs to be taken care of; hypersensitive to negative evaluation Obsessive-compulsive Preoccupied with orderliness, perfectionism, and control

PDs are relatively common, with a prevalence of 10–18% in the general population. Patients with PDs may seek help from family physicians for physical complaints, rather than psychiatric help. Higher rates for all types of PDs are found in medical settings. Prevalence of BPD in the general community is 1.2%. 

PDs have a pervasive impact because they are central to who the person is. They are major sources of long-term disability and are associated with greatly increased mortality. Patients with PDs have fewer coping skills and during stressful situations may have greater difficulties, which are worsened by poor social competency, impulse control, and social support. Patients with BPD are frequently maltreated in the forms of sexual, physical, and emotional abuse; physical neglect; and witnessing violence. PDs are identified in 70–85% of persons identified as criminal, 60–70% of persons with alcohol dependence, and 70–90% of persons who are drug dependent. 

Borderline, schizoid, schizotypal, and dependent PDs are associated with high degrees of functional impairments and greater risk for depression and alcohol abuse. Obsessive-compulsive and narcissistic PDs may not result in appreciable degrees of impairment. Dependent PD is associated with a marked increase in health care utilization. 

Referensi:
Current Diagnosis & Treatment Family Medicine 2nd Edition (McGraw-Hill) 2007